Sleep and information processing in individuals who have sustained a traumatic brain injury

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Abstract

Individuals who have sustained a traumatic brain injury (TBI) often complain of t roubl e
sleeping and daytime fatigue but little is known about the neurophysiological
underpinnings of the s e sleep difficulties. The fragile sleep of thos e with a TBI was
predicted to be characterized by impairments in gating, hyperarousal and a breakdown in
sleep homeostatic mechanisms. To test these hypotheses, 20 individuals with a TBI (18-
64 years old, 10 men) and 20 age-matched controls (18-61 years old, 9 men) took part in
a comprehensive investigation of their sleep. While TBI participants were not recruited
based on sleep complaint, the fmal sample was comprised of individuals with a variety of
sleep complaints, across a range of injury severities. Rigorous screening procedures were
used to reduce potential confounds (e.g., medication). Sleep and waking data were
recorded with a 20-channel montage on three consecutive nights. Results showed
dysregulation in sleep/wake mechanisms. The sleep of individuals with a TBI was less
efficient than that of controls, as measured by sleep architecture variables. There was a
clear breakdown in both spontaneous and evoked K-complexes in those with a TBI.
Greater injury severities were associated with reductions in spindle density, though sleep
spindles in slow wave sleep were longer for individuals with TBI than controls.
Quantitative EEG revealed an impairment in sleep homeostatic mechanisms during sleep
in the TBI group. As well, results showed the presence of hyper arousal based on
quantitative EEG during sleep. In wakefulness, quantitative EEG showed a clear
dissociation in arousal level between TBls with complaints of insomnia and TBls with
daytime fatigue. In addition, ERPs indicated that the experience of hyper arousal in
persons with a TBI was supported by neural evidence, particularly in wakefulness and Stage 2 sleep, and especially for those with insomnia symptoms. ERPs during sleep
suggested that individuals with a TBI experienced impairments in information processing
and sensory gating. Whereas neuropsychological testing and subjective data confirmed
predicted deficits in the waking function of those with a TBI, particularly for those with
more severe injuries, there were few group differences on laboratory computer-based
tasks. Finally, the use of correlation analyses confirmed distinct sleep-wake relationships
for each group. In sum, the mechanisms contributing to sleep disruption in TBI are
particular to this condition, and unique neurobiological mechanisms predict the
experience of insomnia versus daytime fatigue following a TBI. An understanding of
how sleep becomes disrupted after a TBI is important to directing future research and
neurorehabilitation.